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This experiment represents the first in-vivo model of Alzheimer's disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease as a result of a gene-environment interaction.<ref name="Cox and Davis">{{cite journal |vauthors=Cox PA, Davis DA, Mash DC, Metcalf JS, Banack SA | year = 2015 | title = Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain | journal = Proceedings of the Royal Society B | volume = 283 | issue = 1823 | doi = 10.1098/rspb.2015.2397 | pmid = 26791617 | pmc = 4795023 | page=20152397}}</ref> |
This experiment represents the first in-vivo model of Alzheimer's disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease as a result of a gene-environment interaction.<ref name="Cox and Davis">{{cite journal |vauthors=Cox PA, Davis DA, Mash DC, Metcalf JS, Banack SA | year = 2015 | title = Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain | journal = Proceedings of the Royal Society B | volume = 283 | issue = 1823 | doi = 10.1098/rspb.2015.2397 | pmid = 26791617 | pmc = 4795023 | page=20152397}}</ref> |
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Degenerative locomotor diseases have been described in animals grazing on [[cycad]] species, fueling interest in a possible link between the plant and the [[etiology]] of ALS/PDC. Subsequent laboratory investigations discovered the presence of BMAA. BMAA induced severe neurotoxicity in [[rhesus macaques]], including:<ref name=Spencer>{{cite book | last1=Spencer | first1=Peter S. | last2=Hugon | first2=J. | last3=Ludolph | first3=A. | last4=Nunn | first4=P. B. | last5=Ross | first5=S. M. | last6=Roy | first6=D. N. | last7=Schaumburg | first7=H. H.|editor-last1=Bock|editor-first1=Gregory|editor-last2=O'Connor|editor-first2=Maeve | title=Ciba Foundation Symposium 126 |
Degenerative locomotor diseases have been described in animals grazing on [[cycad]] species, fueling interest in a possible link between the plant and the [[etiology]] of ALS/PDC. Subsequent laboratory investigations discovered the presence of BMAA. BMAA induced severe neurotoxicity in [[rhesus macaques]], including:<ref name=Spencer>{{cite book | last1=Spencer | first1=Peter S. | last2=Hugon | first2=J. | last3=Ludolph | first3=A. | last4=Nunn | first4=P. B. | last5=Ross | first5=S. M. | last6=Roy | first6=D. N. | last7=Schaumburg | first7=H. H.|editor-last1=Bock|editor-first1=Gregory|editor-last2=O'Connor|editor-first2=Maeve | title=Ciba Foundation Symposium 126 ‐ Selective Neuronal Death| chapter=14: Discovery and Partial Characterization of Primate Motor-System Toxins | series=Novartis Foundation Symposia | publisher=Wiley Online Library | date=28 September 2007 | volume=126 | issn=1935-4657 | doi=10.1002/9780470513422.ch14| pmid = 3107939 | pages=221–238| isbn=978-0-470-51342-2 }}</ref> |
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*limb muscle [[atrophy]] |
*limb muscle [[atrophy]] |
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*nonreactive degeneration of [[anterior horn cells]] |
*nonreactive degeneration of [[anterior horn cells]] |
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Greek: Ά ά Έ έ Ή ή Ί ί Ό ό Ύ ύ Ώ ώ Α α Β β Γ γ Δ δ Ε ε Ζ ζ Η η Θ θ Ι ι Κ κ Λ λ Μ μ Ν ν Ξ ξ Ο ο Π π Ρ ρ Σ σ ς Τ τ Υ υ Φ φ Χ χ Ψ ψ Ω ω {{Polytonic|}}
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